PTX3, which is also called pentraxin, pentaxin, TSG-14 or MPTX3, is a secretion protein belonging to the pentraxin family and is known to be expressed in human umbilical cord vessel endothelium cells stimulated with interleukin 1 (IL-1) (Non-Patent Document 1).
The pentraxin family includes C-reactive protein (CRP) and serum amyloid P component (SAP), which are known as inflammation-related proteins. Pentraxin is also called long pentraxin, and CRP is also called short pentraxin. Thus, pentraxin is implicative of the presence of a CRP sequence region in the structure thereof, and is predicted to function as an inflammation-related protein. Differing from CRP and SAP, PTX3 is not susceptible to induction by IL-6. The type of cells expressing PTX3 protein differs from those of CRP and SAP. These features indicate that PTX3 also has a function different from that of CRP and SAP (Non-Patent Documents 2 and 3).
In patients of acute myocardial infarction, which is considered a type of inflammation reaction, some PTX3-related findings have been obtained. For example, elevated blood PTX3 level was observed, and PTX3 was detected in plaques present in an advanced arteriosclerotic lesion (possible indicator for small vasculitis) by immunostaining. Thus, PTX3 has been thought to participate in inflammation (Non-Patent Documents 4 to 6).
The term “inflammation” refers to a wide range of types of inflammation including dermatitis and those of a variety of organs. Among them, vasculitis may cause a serious disease such as heart disease or cerebral disease.
Regarding heart disease, risk factors for acute myocardial infarction include high total blood cholesterol, hypertension, diabetes, obesity, and habitual smoking, and efforts to prevent acute myocardial infarction have been made through control of these risk factors. However, according to the “annual dynamic population statistics” (by the Japanese Ministry of Health, Labor, and Welfare (2004)), 15.5% of Japanese die from heart disease, making heart disease the second leading cause of death among Japanese. A detailed study has revealed that most cases of fatal heart diseases are heart failure and acute myocardial infarction, which account for 5.0% and 4.3% of deaths, respectively. These heart diseases are known to be mainly caused by coronary lesion. In addition to heart failure and acute myocardial infarction, examples of complications of coronary lesions include angina and sudden death caused by arrhythmia. In the United States, the American Heart Association has reported that about 12,000,000 or more American people have a clinical history of a certain coronary disease. Thus, coronary lesion is the leading cause of death among Americans, and accounts for about ⅕ of deaths every year.
Examples of cerebral disease include dementia from vasculopathy, and aspirin has been used a prophylactic measure.
Although there are some diagnostic methods for serious pathological conditions in the heart and the brain (e.g., myocardial infarction and cerebral infarction), there has not been known a method for diagnosing mild forms of vasculitis or other vasculopathy.
Conventionally, PTX3 has been determined through an ELISA-based method disclosed in Non-Patent Documents 4 to 6. It is described that PTX3 level reaches its maximum (0.5 to 22 ng/mL) 7.5 hours after myocardial infarction, and then drastically decreases to 0.5 to 2.5 ng/mL, which is a level exhibited by healthy people probably not suffering heart disease. Thus, conventional determination of PTX3 level indicates that the blood PTX3 protein level increases during myocardial infarction attack. However, heretofore, modification in PTX3 protein level at a stage before the onset of myocardial infarction has not yet been elucidated.    Non-Patent Document 1: Breviorio et al.: J. Biol. Chem., 267(31), 22190-7 (1992)    Non-Patent Document 2: J. Biol. Chem., 267(31), 22190-7 (1992)    Non-Patent Document 3: Domyaku Koka (Arteriosclerosis), 24(7-8), 375-80 (1996)    Non-Patent Document 4: Arthritis and Rheumatism, 44/12 (2841-50), 2001    Non-Patent Document 5: Circulation, 102, 636-41 (2000)    Non-Patent Document 6: Arterioscler. Thromb. Vasc. Biol. 2002; 22: e10-e14    Patent Document 1: WO 2005/080981 pamphlet